3D Cell Printed Tissue Analogues: A New Platform for Theranostics

Stem cell theranostics has received much attention for noninvasively monitoring and tracing transplanted therapeutic stem cells through imaging agents and imaging modalities. Despite the excellent regenerative capability of stem cells, their efficacy has been limited due to low cellular retention, low survival rate, and low engraftment after implantation. Three-dimensional (3D) cell printing provides stem cells with the similar architecture and microenvironment of the native tissue and facilitates the generation of a 3D tissue-like construct that exhibits remarkable regenerative capacity and functionality as well as enhanced cell viability. Thus, 3D cell printing can overcome the current concerns of stem cell therapy by delivering the 3D construct to the damaged site. Despite the advantages of 3D cell printing, the in vivo and in vitro tracking and monitoring of the performance of 3D cell printed tissue in a noninvasive and real-time manner have not been thoroughly studied. In this review, we explore the recent progress in 3D cell technology and its applications. Finally, we investigate their potential limitations and suggest future perspectives on 3D cell printing and stem cell theranostics.116Nsciescopu

Enhancement on Radon Adsorption Property of GAC using Nano-size Carbon Colloids

Granular activated carbon (GAC) is well-known as an efficient adsorbent against a number of gaseous pollutants. Radon is one of those pollutants, and radon has been classified as the second leading cause of lung cancer in USA. This study was to enhance the radon removal efficiency with applying nano-technology. Nano-size carbon colloids (NCC) was produced through electrolysis which is simple and cheap. NCC was used for impregnation with activated carbon. Surface areas of both NCC-treated and non-treated activated carbon did not show a significant difference. However, the results of radon removal efficiency show that impregnated carbon with NCC could capture about 1.3 ~ 2 times of more radon gas compared to non-treated activated carbon. It is assumed that nano-size carbon colloids might have filled up meso-pores, and meso-pores turned into micro-pores eventually. Because meso-pores initially accounted for large portion of whole pores, more radon could be captured to NCC-impregnated activated carbon. Keywords: Radon, Nano-Size Carbon Collid, Activated Carbo

Carbon Monoxide Protects against Hepatic Ischemia/Reperfusion Injury via ROS-Dependent Akt Signaling and Inhibition of Glycogen Synthase Kinase 3β

Carbon monoxide (CO) may exert important roles in physiological and pathophysiological states through the regulation of cellular signaling pathways. CO can protect organ tissues from ischemia/reperfusion (I/R) injury by modulating intracellular redox status and by inhibiting inflammatory, apoptotic, and proliferative responses. However, the cellular mechanisms underlying the protective effects of CO in organ I/R injury remain incompletely understood. In this study, a murine model of hepatic warm I/R injury was employed to assess the role of glycogen synthase kinase-3 (GSK3) and phosphatidylinositol 3-kinase (PI3K)-dependent signaling pathways in the protective effects of CO against inflammation and injury. Inhibition of GSK3 through the PI3K/Akt pathway played a crucial role in CO-mediated protection. CO treatment increased the phosphorylation of Akt and GSK3-beta (GSK3β) in the liver after I/R injury. Furthermore, administration of LY294002, an inhibitor of PI3K, compromised the protective effect of CO and decreased the level of phospho-GSK3β after I/R injury. These results suggest that CO protects against liver damage by maintaining GSK3β phosphorylation, which may be mediated by the PI3K/Akt signaling pathway. Our study provides additional support for the therapeutic potential of CO in organ injury and identifies GSK3β as a therapeutic target for CO in the amelioration of hepatic injury

A Multimodal Deep Learning-Based Fault Detection Model for a Plastic Injection Molding Process

The authors of this work propose a deep learning-based fault detection model that can be implemented in the field of plastic injection molding. Compared to conventional approaches to fault detection in this domain, recent deep learning approaches prove useful for on-site problems involving complex underlying dynamics with a large number of variables. In addition, the advent of advanced sensors that generate data types in multiple modalities prompts the need for multimodal learning with deep neural networks to detect faults. This process is able to facilitate information from various modalities in an end-to-end learning fashion. The proposed deep learning-based approach opts for an early fusion scheme, in which the low-level feature representations of modalities are combined. A case study involving real-world data, obtained from a car parts company and related to a car window side molding process, validates that the proposed model outperforms late fusion methods and conventional models in solving the problem

Decreased expression of extracellular matrix proteins and trophic factors in the amygdala complex of depressed mice after chronic immobilization stress

BACKGROUND: The amygdala plays an essential role in controlling emotional behaviors and has numerous connections to other brain regions. The functional role of the amygdala has been highlighted by various studies of stress-induced behavioral changes. Here we investigated gene expression changes in the amygdala in the chronic immobilization stress (CIS)-induced depression model. RESULTS: Eight genes were decreased in the amygdala of CIS mice, including genes for neurotrophic factors and extracellular matrix proteins. Among these, osteoglycin, fibromodulin, insulin-like growth factor 2 (Igf2), and insulin-like growth factor binding protein 2 (Igfbp2) were further analyzed for histological expression changes. The expression of osteoglycin and fibromodulin simultaneously decreased in the medial, basolateral, and central amygdala regions. However, Igf2 and Igfbp2 decreased specifically in the central nucleus of the amygdala. Interestingly, this decrease was found only in the amygdala of mice showing higher immobility, but not in mice displaying lower immobility, although the CIS regimen was the same for both groups. CONCLUSIONS: These results suggest that the responsiveness of the amygdala may play a role in the sensitivity of CIS-induced behavioral changes in mice

Janus-faced Sestrin2 controls ROS and mTOR signalling through two separate functional domains

Sestrins are stress-inducible metabolic regulators with two seemingly unrelated but physiologically important functions: reduction of reactive oxygen species (ROS) and inhibition of the mechanistic target of rapamycin complex 1 (mTORC1). How Sestrins fulfil this dual role has remained elusive so far. Here we report the crystal structure of human Sestrin2 (hSesn2), and show that hSesn2 is twofold pseudo-symmetric with two globular subdomains, which are structurally similar but functionally distinct from each other. While the N-terminal domain (Sesn-A) reduces alkylhydroperoxide radicals through its helix–turn–helix oxidoreductase motif, the C-terminal domain (Sesn-C) modified this motif to accommodate physical interaction with GATOR2 and subsequent inhibition of mTORC1. These findings clarify the molecular mechanism of how Sestrins can attenuate degenerative processes such as aging and diabetes by acting as a simultaneous inhibitor of ROS accumulation and mTORC1 activation

Kaempferol inhibits IL‑1β‑induced proliferation of rheumatoid arthritis synovial fibroblasts and the production of COX‑2, PGE2 and MMPs

Inflammatory cytokines, matrix metalloproteinases (MMPs) and cyclooxygenase (COX)‑2 released from rheumatoid arthritis synovial fibroblasts (RASFs) are involved in the destruction of both articular bone and cartilage. Kaempferol has been reported to act as an antioxidant and anti‑inflammatory agent by inhibiting nitric oxide synthase and COX enzymes. The aim of the present study was to determine the effects of kaempferol on the interleukin‑1β (IL‑1β)‑induced proliferation of RASFs and the production of MMPs, COX and prostaglandin E2 (PGE2) by RASFs. The proliferation of the RASFs stimulated with IL‑1β and treated with/without kaempferol was evaluated by CCK‑8 assay. The expression of MMPs, TIMP metallopeptidase inhibitor‑1 (TIMP‑1), COXs, PGE2 and that of intracellular MAPK signaling molecules, including p‑ERK, p‑p38, p‑JNK and nuclear factor‑κB (NF‑κB) was examined by immunoblotting or semi‑quantitative reverse transcription‑polymerase chain reaction (RT‑PCR) and ELISA under the conditions described above. Kaempferol inhibited the proliferation of both unstimulated and IL‑1β‑stimulated RASFs, as well as the mRNA and protein expression of MMP‑1, MMP-3, COX‑2 and PGE2 induced by IL‑1β. Kaempferol also inhibited the phosphorylation of ERK‑1/2, p38 and JNK, as well as the activation of NF‑κB induced by IL‑1β. These results indicate that kaempferol inhibits synovial fibroblast proliferation, as well as the production of and MMPs, COX‑2 and PGE2, which is involved in articular inflammation and destruction in rheumatoid arthritis (RA). Our data suggest that kaempferol may be a novel therapeutic agent for the treatment of RA